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Zapytanie: FERRARI-LACRAZ
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Tytuł oryginału: Fibroblast-like synoviocytes from rheumatoid arthritis patients express functional IL-15 receptor complex: endogenous IL-15 in autocrine faschion enhances cell proliferation and expression of Bcl-xL and Bcl-2.
Autorzy: Kurowska Mariola, Rudnicka Weronika, Kontny Ewa, Janicka Iwona, Chorazy Magdalena, Kowalczewski Jacek, Ziółkowska Maria, Ferrari-Lacraz Sylvie, Strom Terry B., Maśliński Włodzimierz
Źródło: J. Immunol. 2002: 169 (4) s.1760-1767, il., bibliogr. 49 poz.
Sygnatura GBL: 300,982

Hasła klasyfikacyjne GBL:
  • reumatologia

    Typ dokumentu:
  • praca kliniczna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: The hallmarks of rheumatoid arthritis (RA) are leukocytic infiltratin of the synovium and expansiveness of fibroblast-like synovicytes (FLS). The abnormal proliferation of FLS and their resistance to apoptosis is mediated, at least in part, bay present in RA joints proinflammatory cytokines and growth factors. Because IL-15 exerts properties of antiapoptotic and growth facators, and is produced by RA FLS, we hypothesized that IL-15 participates in RA FLA activation. To test this hypothesis, we first examined whether RA FLS express chains required for high affinity functional IL-15R. Indeed, RA FLS express IL-15Rŕ at mRNA and protein levels. Moreover, we confirmed the presence of IL-2Rá and common ç-chains. Interstingly, TNF-ŕ or IL-1á triggered significant elevation of IL-15Rŕ chanin at mRNA and protein levels. Next, we investigated the effects of exogenous or endogenous IL-15 on Bcl-2 andBcl-XL expression, FLS proliferation, and apoptosis. Exogenous IL-15 enhanced RA FLS proliferation and increased the level of mRNA-encoding Bcl-XL. To test the role of endogenous IL-15 in the activation of RA FLS, an IL-15 mutant/Fcç2a protein exerting properties of specific antagonist to the IL-15Rŕ chain was used. We found that blocking IL-15 biological activities using this protein substantially reduced endogenous expression of Bcl-2 and Bcl-XL, and RA FLA proliferation that was reflected by increased apoptosis. Thus, we havae demonstrated that a distinctive phenotype of RA FLS, i.e., persistent activation, proliferation, and resistance to apoptosis, is related to the autocrine activation of IL-15Rs by FLS-derived IL-15.

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